For at least a decade it has been thought that microbial molecular mimics might play a role in the development of autoimmune diseases. Until recently, however, viral molecular mimicry had not been implicated in the etiology of an autoimmune disease that follows a natural viral infection. Studies in the Cantor laboratory provided the first such evidence when they showed that a peptide derived from the HSV-1 virion-associated protein UL6 acts as a molecular mimic in the development of Herpes Stromal Keratitis (HSK), an autoimmune disorder that results from corneal infection by HSV1. However, the extent to which viral molecular mimicry plays a role in the development of HSK is still unknown since many aspects of the mechanism remain poorly understood. Experiments using transgenic mice expressing a single TCR and mutant HSV-1 strains that are replication competent but lack the UL6 mimic should indicate whether T cell recognition of the UL6 epitope is sufficient and/or essential in the development of HSK, as well as, what other aspects, if any, of viral infection are important for the development of HSK. Furthermore, the identification of the self-antigen in the murine HSK system could have clinical implications for people suffering from ocular herpes infections.